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Purpose of Review <p>Pulmonary surfactant protein B (SFTPB) is a lung-specific protein essential for surfactant function. This review summarizes its biology, circulation during pulmonary injury, association with high-density lipoprotein (HDL), and emerging links to cardiovascular disease (CVD).</p> Recent Findings <p>Alveolar–capillary barrier disruption in heart failure, valvular disease, acute respiratory distress syndrome, and smoking permits immature SFTPB (pro-SFTPB) to enter the bloodstream. Circulating pro-SFTPB binds predominantly to HDL, impairing antioxidant capacity while largely preserving cholesterol efflux and endothelial anti-inflammatory functions. HDL-bound SFTPB reflects pulmonary–vascular stress and predicts incident CVD independently of traditional risk factors.</p> Summary <p>These observations support a “lung–HDL–vascular” axis in which alveolar–capillary injury is encoded in circulating HDL. SFTPB functions as a sensitive biomarker of lung–vascular crosstalk, and future studies should clarify its functional relevance, temporal dynamics, and translational potential.</p>

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Surfactant Protein B and the Lung–HDL–Vascular Axis: Linking Pulmonary Injury to Cardiovascular Risk

  • 期刊论文

  • 发表日期：

    2026年2月20日

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  • Baohai Shao

摘要

Purpose of Review

Pulmonary surfactant protein B (SFTPB) is a lung-specific protein essential for surfactant function. This review summarizes its biology, circulation during pulmonary injury, association with high-density lipoprotein (HDL), and emerging links to cardiovascular disease (CVD).

Recent Findings

Alveolar–capillary barrier disruption in heart failure, valvular disease, acute respiratory distress syndrome, and smoking permits immature SFTPB (pro-SFTPB) to enter the bloodstream. Circulating pro-SFTPB binds predominantly to HDL, impairing antioxidant capacity while largely preserving cholesterol efflux and endothelial anti-inflammatory functions. HDL-bound SFTPB reflects pulmonary–vascular stress and predicts incident CVD independently of traditional risk factors.

Summary

These observations support a “lung–HDL–vascular” axis in which alveolar–capillary injury is encoded in circulating HDL. SFTPB functions as a sensitive biomarker of lung–vascular crosstalk, and future studies should clarify its functional relevance, temporal dynamics, and translational potential.